Poly(ADP-ribose) metabolism appears normal in EM9, a mutagen-sensitive mutant of CHO cells

Miyoko Ikejima; Dian Bohannon; D. Michael Gill; Larry H. Thompson

doi:10.1016/0027-5107(84)90109-X

Poly(ADP-ribose) metabolism appears normal in EM9, a mutagen-sensitive mutant of CHO cells

Miyoko Ikejima, Dian Bohannon, D. Michael Gill, Larry H. Thompson

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

EM9 is a mutagen-sensitive CHO cell whose phenotype resembles that of normal CHO cells exposed to 3-aminobenzamide, an inhibitor of poly(ADP-ribose) synthesis. This phenotype suggested that EM9 might be defective in poly(ADP-ribose) metabolism, but we now cannot find any abnormality in the synthesis or in the degradation of poly(ADP-ribose) in permeabilized EM9 cells. Thus the effects of 3-aminobenzamide on wild-type cells may be due to the inhibition of processes other than poly(ADP-ribose) synthesis. 3-Aminobenzamide enhances the cytotoxicity of EMS toward EM9 and control cells to the same degree.

Original language	English (US)
Pages (from-to)	213-220
Number of pages	8
Journal	Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Volume	128
Issue number	2
DOIs	https://doi.org/10.1016/0027-5107(84)90109-X
State	Published - 1984
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Health, Toxicology and Mutagenesis
Medicine(all)

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title = "Poly(ADP-ribose) metabolism appears normal in EM9, a mutagen-sensitive mutant of CHO cells",

abstract = "EM9 is a mutagen-sensitive CHO cell whose phenotype resembles that of normal CHO cells exposed to 3-aminobenzamide, an inhibitor of poly(ADP-ribose) synthesis. This phenotype suggested that EM9 might be defective in poly(ADP-ribose) metabolism, but we now cannot find any abnormality in the synthesis or in the degradation of poly(ADP-ribose) in permeabilized EM9 cells. Thus the effects of 3-aminobenzamide on wild-type cells may be due to the inhibition of processes other than poly(ADP-ribose) synthesis. 3-Aminobenzamide enhances the cytotoxicity of EMS toward EM9 and control cells to the same degree.",

author = "Miyoko Ikejima and Dian Bohannon and {Michael Gill}, D. and Thompson, {Larry H.}",

year = "1984",

doi = "10.1016/0027-5107(84)90109-X",

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T1 - Poly(ADP-ribose) metabolism appears normal in EM9, a mutagen-sensitive mutant of CHO cells

AU - Ikejima, Miyoko

AU - Bohannon, Dian

AU - Michael Gill, D.

AU - Thompson, Larry H.

PY - 1984

Y1 - 1984

N2 - EM9 is a mutagen-sensitive CHO cell whose phenotype resembles that of normal CHO cells exposed to 3-aminobenzamide, an inhibitor of poly(ADP-ribose) synthesis. This phenotype suggested that EM9 might be defective in poly(ADP-ribose) metabolism, but we now cannot find any abnormality in the synthesis or in the degradation of poly(ADP-ribose) in permeabilized EM9 cells. Thus the effects of 3-aminobenzamide on wild-type cells may be due to the inhibition of processes other than poly(ADP-ribose) synthesis. 3-Aminobenzamide enhances the cytotoxicity of EMS toward EM9 and control cells to the same degree.

AB - EM9 is a mutagen-sensitive CHO cell whose phenotype resembles that of normal CHO cells exposed to 3-aminobenzamide, an inhibitor of poly(ADP-ribose) synthesis. This phenotype suggested that EM9 might be defective in poly(ADP-ribose) metabolism, but we now cannot find any abnormality in the synthesis or in the degradation of poly(ADP-ribose) in permeabilized EM9 cells. Thus the effects of 3-aminobenzamide on wild-type cells may be due to the inhibition of processes other than poly(ADP-ribose) synthesis. 3-Aminobenzamide enhances the cytotoxicity of EMS toward EM9 and control cells to the same degree.

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